(1) Bio-microscopy of bulbar conjunctiva and examination of the punch biopsy of synovial membrane demonstrated various kinds of blood vessel lesions in rheumatic fever and rheumatic heart disease.
(2) These lesions were observed not only in cases with manifestations of rheumatic changes, but with no apparent clinical and laboratory evidence of rheumatic activity, too. It would be suggested that laboratory tests of the present day were not sensitive enough to indicate the presence of mild rheumatic inflammation. Incidious morphologic changes of blood vessels might exist in rheumatic heart disease patients with no evidence of rheumatic activity.
(3) The prevention and treatment of those vascular lesions are important, since the vascular changes can accelerate aging degenerative process of blood vessels to bring out early appearance of arteriosclerosis, and can also cause various damages to organs and tissues, which are ischemic injuries due to anoxemia.

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The precordial low-frequency vibrocardiograms of 82 systemic hypertensive cases were investigated and analyzed in detail comparing with the normal.
(1) The patterns of tracings in hypertension were classified into two types as in the normal. However, type II was observed more frequently than type I. Both types were characterized by prominent "E" (ejection upstroke), increased "AU" (atrial upstroke) and marked "B" (midsystolic bulge).
(2) The forceful apical impulse in hypertension was expressed as the prominent "E". This "E" was markedly exaggerated by cold pressor test. Therefore, the "E" was the expression of left ventricular strain in both organic and functional senses. Moreover, the sustained heaving apical impulse was caused by prominent "E" followed by marked "B" seen in cases with severe hypertension.
(3) The increased "A" meant the exaggerated left atrial movement in hypertensive cases as indicated by the accentuated atrial sound in the phonocardiogram and the P-wave changes in the electrocardiogram. This change was so sensitive to deterioration or improvement of the diseased state that it was one of the most useful signs which indicated the impending or established congestive heart failure in hypertension. The cold pressor test showed an exaggeration of "AU", indicating this atrial motion was caused by abnormal ventricular filling during atrial activity, as seen in the cases of accentuated atrial sound.
(4) The mid-systolic bulge (B) was recorded prominently in severe cases particularly in cases with prominent "E". This bulge was caused by left ventricular hypertrophy as well as myocardial damage, and exaggerated by cold pressor test particularly in the cases with marked cardiac impairment. This meant that the "B" was a senstiive index of myocardial insufficiency which was accompanied by this pathologic conditions.
(5) In order to obtain the meanings of each movement, cold pressor test and the follow-up study were performed. The possible mechanism of each deflection and the clinical usefulness of these tracings were fully discussed based on our observations in addition to the previously reported contributions in this field. It was concluded that the precordial lowfrequency vibrocardiogram was one of the most sensitive and the useful methods in order to estimate the objective state of cardiac function and to elucidate some of the circulatory disturbances in hypertensive heart.

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(1) Intramuscular coronary arterial (I.M.C.A.) (80-500μ) sclerosis as a cause of myocardial disease was studied pathologically.
(2) I.M.C.A. sclerosis was found in high incidence in the cases over 40 years of age, and the tendency of stenosis of the vessels with the lesions increased with age.
(3) The lesions was independent of atherosclerosis of the coronary arterial stem or ante-mortem hypertension.
(4) Severe lesions of this type was considered to be a cause of definite myocardial lesions without atherosclerosis in the coronary arterial stem, and its clinical feature seemed to be a cardiac decompensation without anginal pain.
(5) In addition to atherosclerosis of the coronary arterial stem, I.M.C.A. sclerosis could be an important cause of coronary heart disease, especially in people with a low grade of atherosclerosis such as the Japanese.

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(1) Investigation was made on 283 cases which were decided as "acute cardiac death of unknown etiology" (the so called "Pokkuri disease" in Japanese) by autopsy at the Tokyo Medical Examiner Office.
(2) Apparently healthy young males were most common among the groups and they died abruptly during sleep at night. The cause of death was not found by autopsy or biochemical examination.
(3) Our subjects were different from the "acute cardiac sudden death of unknown etiology" reported in Europe and America. Deaths similar to that found in our country are not reported in such countries.
(4) From our study, the neurohumoral system, especially the adrenal gland and the autonomic nervous system appear to play an important role in the causative mechanism of "acute cardiac death of unknown etiology."

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The change in the heart rate and arrhythmias produced by electrical stimulation of the brain stem of dogs were observed and analyzed.
The results are as follows ;
(1) In the early phase of the stimulation, sinus tachycardia was mostly observed, especially marked on the stimulation of the posterior part in the hypothalamus, the midline, ventral and medial nuclei groups in the thalamus and the posterior commissure, the central gray stratum and a part of reticular formation in the midbrain. Sinus bradycardia was infrequent and not so marked.
(2) In the late phase or after the end of the stimulation, bradycardia was often observed and sometimes accompanied by such arrhythmias as atrioventricular block, nodal escaped beat or nodal escaped rhythm. This phenomenon was marked especially when blood pressure was elevated remarkably. It was explained mainly as vagal reflex, partly delayed vagal reaction of the stimulated area.
(3) Ventricular extrasystole induced by central nervous stimulation was classified into 2 groups 'A' and 'B', according to the mode of appearance. The extrasystole of type 'A' appeared in the early phase of the stimulation, independently upon elevation of the blood pressure and was perhaps of right ventricular origin. The extrasystole of type 'B', the appearance of which was similar to that of escaped beat (that is, of longer coupling), occurred in the late phase or after the cessation of the stimulation, associated with a blood pressure elevation and was thought to be of left ventricular origin. While the extrasystole of type 'A' seems to be of direct central nervous origin, the one of type 'B' is considered of secondary nature.
(4) The distribution of the area participating with the extrasystole of type 'A' was relatively restricted to the median portion of the brain stem. These area may have some function to influence the heart to produce ventricular extrasystoles.

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Transmembrane potentials and the process of excitation propagation of the rabbit's and canine heart in the A-V node and its vicinity were studied by means of the microelectrode method.
(1) In the vicinity of the A-V node, no action potential showing the slow diastolic depolarization was obtained.
The configuration of the action potential recorded from this area exhibited a tracing similar to that of the action potential recorded from the atrial ordinary muscle.
(2) It was inferred that the right and septal branches of the crista terminalis extended into the atrial tissue near the vicinity of the A-V node. In these areas the arrival times of the excitation through both branches of the crista terminalis were almost the same.
(3) It was impossible to clarify whether the excitation through the crista terminalis activated the A-V node or whether it was activated by the excitation through some specialized muscle, in which the conduction rate was slower than that of the crista terminalis.
(4) The configuration of the transmembrane potential of the A-V node was peculiar.
The transmembrane potential recorded from the atrial tissue in the A-V node adjacent to the S-A node was characterized by a slow diastolic depolarization, a low resting potential, a very gentle upstroke of the depolarization phase and a lack of overshoot and plateau.
When the penetration approached the tissue close to the His bundle, the action potential began to show a plateau and a rather rapid upstroke of the depolarization phase.
(5) A marked delay was observed in the area between the atrial ordinary muscle close to the A-V node and the tissue in the A-V node adjacent to the S-A node.
The conduction rate in this area was 0.03∼0.025M./sec.

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In a series of ECGs which had been recorded with a patient suffering from the Stokes-Adams syndrome, we observed 3 types of the QRS complex accompanied by various degrees of the A-V block; A) pattern of the left bundle branch block, B) pattern of the right bundle branch block and C) normal QRS complex.
Analyses of these QRS complexes and P-Q intervals were carried out by means of the 12 leads ECG and Takayasu's orthogonal VCG. And genesis of these QRS complexes could be well explained applying the concept of the accelerated conduction theory presented by Prinzmetal.

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